Abacavir Use Research Articles

Abacavir exposure and cardiovascular risk factors in HIV-positive patients with coronary heart disease: a retrospective case–control study

HIV-positive patients have an estimated twofold increased risk of acute myocardial infarction and coronary heart disease (CHD). While traditional cardiovascular risk factors and the effects of HIV and chronic inflammation all play a role, the contribution of long-term exposure to antiretroviral (ARV) agents is becoming clear. We performed a retrospective case-control study of HIV-positive patients seen from January 1996 to December 2009 to evaluate the impact of HIV suppression and exposure to specific ARVs on the incidence of CHD. Cases (n=68) were HIV-positive with evidence of CHD. Two age- and sex-matched HIV-positive controls (n=136) without a diagnosis of CHD were assigned for each case. The cumulative incidence of CHD in the period covered by the study was 3.8%, with an incidence of 8.5 cases per 1000 patient-years of follow up. Cases had an increased likelihood of having hypertension (odds ratio (OR): 6.62, P<0.001), a family history of CHD (OR: 5.82, P<0.001), lower high-density lipoprotein levels (OR: 0.28, P=0.025) and higher Framingham risk scores compared with controls. Following adjustment for traditional cardiovascular risk factors, the presence of CHD was significantly associated with the current use of abacavir (OR: 2.10, P=0.03). Protease inhibitor therapy, HIV viral load and duration of known HIV infection were not predictive of CHD in our patient population. Our data add to the evidence that abacavir use is associated with CHD in HIV-positive patients in Australia.

Abacavir/Lamivudine Fixed-Dose Combination With Ritonavir-Boosted Darunavir: A Safe and Efficacious Regimen for HIV Therapy

Background: Current treatment guidelines recommend the use of tenofovir (TDF) and emtricitabine (FTC) along with a third agent to treat HIV-positive adults. However, other treatment options, including the use of abacavir (ABC) and lamivudine (3TC) when used with ritonavir-boosted darunavir (DRV/r), have rarely been studied. Objective: We evaluated the safety and efficacy of the coformulation of ABC/3TC administered with DRV/r in treatment-naïve and treatment-experienced patients. Methods: HIV-infected adults who received an open-label combination of ABC/3TC/ DRV/r were followed in a community clinic in Montréal. Patients had no resistance to any of the compounds in their regimen. Viral load (VL), CD4 cell count, AST, ALT, and creatinine levels were examined throughout the 48 weeks of follow-up. Results: Sixty-seven patients with a mean age of 45 years were enrolled. Two did not return for follow-up and were excluded. Thirty-five (52%) were treatment- experienced and the remaining were treatment-naïve. HLA-B*5701 test results were available for 56 patients and none were positive. At baseline, mean VL was 4.8 log for treatment-naïve and 2.3 log for experienced patients. Twelve patients discontinued the study regimen prior to reaching the endpoint. At week 48, 79% had a VL <50. Median CD4 cell gain was higher among treatment-naïve patients (273 cells) than among treatment-experienced patients (102 cells) (P = .002). No patient experienced any grade 2 or higher liver enzyme elevation throughout the study. Conclusions: The new combination of ABC/3TC/DRV/r demonstrates a high rate of antiviral activity with no major toxicity. The drug combination appears to be generally safe and well tolerated.

A randomized controlled trial assessing the effects of raltegravir intensification on endothelial function in treated HIV infection.

To determine whether intensification with raltegravir improves endothelial function in antiretroviral-treated HIV-infected individuals. : Randomized, double-blinded, placebo-controlled study. Fifty-six subjects with treatment-mediated viral suppression for at least 1 year were randomized to add 400 mg of raltegravir twice daily or matching placebo for 24 weeks. The primary endpoint was the difference in rate of change in endothelial function [as assessed by flow-mediated vasodilation (FMD) of the brachial artery] from baseline to week 24 between the raltegravir and placebo groups. Linear mixed models were used to evaluate the association of treatment group with changes in FMD, immune activation, and measures of viral persistence. At baseline, the median CD4 T-cell count was 498 cells/mm, nadir CD4 T-cell count was 191 cells/mm, duration of HIV infection was 18 years, FMD was 3.3%, and hyperemic velocity (a marker of microvascular function) was 68.3 cm. There were no significant differences between treatment groups in rate of change in FMD (raltegravir group: +0.032% per week, placebo group: +0.023% per week; P = 0.60). There were also no differences between treatment groups in rate of change in hyperemic velocity, immune activation, or viral persistence. In multivariable analysis, older age, longer duration of HIV infection, and current abacavir use were associated with lower FMD. Lower CD4 T-cell count and current abacavir use were associated with lower hyperemic velocity. The addition of raltegravir to suppressive antiretroviral therapy did not have a significant impact on cardiovascular risk, as assessed by endothelial function (ClinicalTrials.gov NCT00843713).

Cardiovascular risk factors and carotid intima‐media thickness are associated with lower cognitive performance in HIV‐infected patients

The aim of the study was to investigate the relationship between metabolic comorbidities, cardiovascular risk factors or common carotid intima-media thickness (cIMT) and cognitive performance in HIV-infected patients. Asymptomatic HIV-infected subjects were consecutively enrolled during routine out-patient visits at two clinical centres. All patients underwent an extensive neuropsychological battery and assessment of metabolic comorbidities and cardiovascular risk factors. Moreover, cIMT was assessed by ultrasonography. Cognitive performance was evaluated by calculating a global cognitive impairment (GCI) score obtained by summing scores assigned to each test (0 if normal and 1 if pathological). A total of 245 patients (median age 46 years; 84.1% with HIV RNA < 50 copies/mL; median CD4 count 527 cells/μL) were enrolled in the study. Cardiovascular risk factors were highly prevalent in our population: the most frequent were dyslipidaemia (61.2%), cigarette smoking (54.3%) and hypertension (15.1%). cIMT was abnormal (≥ 0.9mm) in 31.8% of patients. Overall, the median GCI score was 2 [interquartile range (IQR) 1-4]; it was higher in patients with diabetes (P = 0.004), hypertension (P = 0.030) or cIMT ≥ 0.9 mm (P < 0.001). In multivariate analysis, it was confirmed that diabetes (P = 0.007) and cIMT ≥ 0.9 mm (P = 0.044) had an independent association with lower cognitive performance. In an analysis of patients on combination antiretroviral therapy (cART), abacavir use was independently associated with a better cognitive performance (P = 0.011), while no association was observed for other drugs or neuroeffectiveness score. Diabetes, cardiovascular risk factors and cIMT showed a strong association with lower cognitive performance, suggesting that metabolic comorbidities could play a relevant role in the pathogenesis of HIV-associated neurocognitive disorders in the recent cART era.

Estimated use of abacavir among adults and children enrolled in public sector antiretroviral therapy programmes in Gauteng, South Africa

Estimated use of abacavir among adults and children enrolled in public sector antiretroviral therapy programmes in Gauteng, South Africa

Estimated use of abacavir among adults and children enrolled in public sector antiretroviral therapy programmes in Gauteng, South Africa

In South Africa, abacavir (ABC) is currently recommended as part of first- and second-line antiretroviral therapy (ART) for HIV-positive paediatric patients. Concerns about overprescribing of the drug, particularly to adults, led to an analysis of ABC use in public sector ART programmes. We investigated current prescription of the drug to adults and children accessing ART in 4 public sector programmes across Gauteng Province, South Africa. ABC was almost exclusively prescribed to children initiating ART and adults requiring regimen changes due to drug toxicities. Patterns of ABC use among HIV-positive paediatric patients followed national ART treatment guidelines on the application of the drug. Although ABC is commonly used in the private sector for adults, the current national ART treatment guidelines for adults and adolescents should include ABC as an alternative to standard first- or second-line ART.

5.0 What to start

5.0 What to start

Low prevalence of HLA B5701 among HIV-infected Thai children in Thailand and Cambodia; implication for abacavir use

Background: There was limited data on diet and life style of dolescents with vertically-transmitted HIV infection. Multifactoial factors affect on weight, height and bone density in this age roup especially dietary intake, exercise and antiretroviralmedicaions. This study aimed to report on the dietary intakes andphysical ctivity in this adolescent group. Methods: We conducted a cross-sectional study using selfeport questionnaires on dietary intake and exercise among IV-infected adolescents. The dietary intake was analysed using NMUCAL-Nutrients program, Database WD4.4. 2010 (Institute of utrition, Mahidol University). The weight for age Z-score and eight for age Z-score were analyzed using Thai reference. The tandard dietary reference intake (DRI) for energywas 2,100-2,300 alories for male and 1,800-1,850 calories for female, and calcium as 1,000mg/day in this age group. General recommendation sugested at least 1 hour/day of physical activity. Results: The study included 101 HIV-infected adolescents, 50% ere male. The mean (SD) of age was 14.6 (1.9) years. The mean SD) of body mass index was 18 (2.8), weight Z-score (WAZ) was 0.76 (1.2), height Z-score (HAZ) was -1.0 (1.2). Number of adoescents who had WAZ< -1.5 SD was 33 and HAZ< -1.5 SD was 34. ean (SD) of caloric and calcium intake were 1,559 (440) kcal/day nd 635 (337)mg/day, respectively. Percentage of adolescentswho ook adequate calorie and calcium and protein as recommended by RI were only 19%, 17% and 69%, respectively. Mean (SD) weightearing exercise was 5.9 (6.4) hours/week and non-weight bearing xercise was 3.1 (4.5) hours/week. Conclusion: The majority of adolescents did not reach DRI for aloric and calcium intake. Clinician should encourage the imporant of dietary intake and exercise for this group of patients. upplement calcium in growing adolescent should be considered.

Prevalence of chronic kidney disease in older patients with HIV infection on antiretroviral treatment

BackgroundRenal insufficiency may affect up to 10% of HIV patients as a result of HIV-associated nephropathy (HIVAN), a consequence of HIV replication in the kidney, AIDS-related kidney disease or drug...

Clinical pharmacogenetics implementation consortium guidelines for HLA-B genotype and abacavir dosing.

Human leukocyte antigen B (HLA-B) is responsible for presenting peptides to immune cells and plays a critical role in normal immune recognition of pathogens. A variant allele, HLA-B*57:01, is associated with increased risk of a hypersensitivity reaction to the anti-HIV drug abacavir. In the absence of genetic prescreening, hypersensitivity affects ~6% of patients and can be life-threatening with repeated dosing. We provide recommendations (updated periodically at http://www.pharmkgb.org) for the use of abacavir based on HLA-B genotype.

Estimated use of abacavir among adults and children enrolled in public sector antiretroviral therapy programmes in Gauteng, South Africa

Estimated use of abacavir among adults and children enrolled in public sector antiretroviral therapy programmes in Gauteng, South Africa

Abacavir, Didanosine and Tenofovir do not Induce Inflammatory, Apoptotic or Oxidative Stress Genes in Coronary Endothelial Cells

The use of abacavir and didanosine in HAART has been associated with an increased risk of myocardial infarction in HIV-infected patients. The aim of this study was to address the development of endothelial dysfunction in cultivated coronary artery endothelial cells (HCAECs) in response to abacavir, didanosine and tenofovir. We examined the impact of these drugs on the expression levels of the proinflammatory, oxidative stress and apoptosis regulating genes in HCAECs. We tested gene and protein expression changes in HCAECs in response to abacavir, didanosine and tenofovir using quantitative real-time reverse transciptase PCR, FACS and ELISA. The assessed genes/proteins included the proinflammatory molecules VCAM-1, ICAM-1, MCP-1, RANTES and IL-6. In addition, we assessed the gene expression of the intracellular reactive oxygen producing NADPH oxidase subunit gp91(PHOX) and the apoptosis regulating molecules Bcl-2 and BAD. Exposure of HCAECs to abacavir, didanosine and tenofovir resulted in no statistically significant changes in any of the tested genes/proteins at any time point or at any concentration. We found no evidence that abacavir, didanosine or tenofovir had direct in vitro effects on coronary endothelial cell gene transcription and protein expression of the selected mediators. If abacavir or didanosine increase cardiovascular risk, it is likely not through the direct endothelial activation pathways tested in these experiments. However, further studies are needed to completely exclude the toxicity of abacavir or didanosine on endothelial cells.

Use of patch testing for the diagnosis of abacavir-related hypersensitivity reaction in HIV patients

The use of antiretroviral drug abacavir (ABC) has been often associated with cutaneous hypersensitivity reactions, the majority being severe. The present study discusses the issues of patch testing associated with pharmacogenetic screening in light of the development of abacavir hypersensitivity reactions (HSRs). The present authors classified 100 patients into three groups: 20 patients (group A) had experienced a hypersensitivity reaction when treated with highly active antiretroviral therapy (HAART) including ABC; 60 HIV-positive patients (group B) were receiving HAART scheme including ABC; 20 HIV-negative patients acted as control group (group C). Patients of group A and B were patch tested with ABC as such, then with an ABC extract diluted to 1 and 10% in petrolatum. Group C patients underwent patches with petrolatum only. A biopsy of the lesion was performed in those patients who showed a positive skin reaction. All patients had been tested for HLA-B5701. A correlation between positive ABC-patch testing and HLA-B5701 was found in 50% of patients enrolled in group A, while in group B and C, all patients tested negative for both genetic marker and ABC-patch testing. Histopathology findings confirmed a vigorous CD4+ and CD8+ cellular response that is compatible with HSR. Patch testing is a safe and sensitive method that can be used for to confirm or exclude any correlation between abacavir and hypersensitivity skin reactions in patients who have been previously treated with abacavir during HAART. Correlation between patch test, immunohistochimical, and genetic tests results shows that genetic testing increases the possibility to identify patients with a true reaction.

Abacavir use and cardiovascular disease events

The use of abacavir (ABC) has been associated with an increased risk of cardiovascular disease in some cohort studies. However, no excess risk of myocardial infarction (MI) with ABC therapy has been observed in individual randomized clinical trials (RCTs) and in the aggregated clinical trials database maintained by the manufacturer of ABC. To combine all the evidence from RCTs by means of meta-analysis to estimate the effect of combined antiretroviral therapy (cART) containing ABC on MI and overall major cardiovascular events (CVEs). Primary outcomes included MI, CVE, adverse events requiring discontinuation of treatment, and overall mortality. We used a conventional Mantel-Haenszel method, with risk ratio and 95% confidence intervals (CIs) or, in the presence of heterogeneity, a random-effect model. Data were from 28 primary RCTs (9233 participants) comparing ABC-containing cART (4376 participants) to other regimens not containing ABC (4857 controls). MI data were available from 18 trials (31 episodes in 7054 patients) and CVE data from 20 trials (79 episodes in 7899 patients). Compared to the controls, ABC use did not increase significantly the occurrence of MI (risk ratio 0.73, 95% CI 0.39-1.35; P = 0.31), CVE (risk ratio 0.95, 95% CI 0.62-1.44; P = 0.80), overall mortality (risk ratio 1.20, 95% CI 0.63-2.27; P = 0.58), and adverse events requiring discontinuation of treatment (risk ratio 0.82, 95% CI 0.67-1.00; P = 0.05). This meta-analysis of RCTs does not support the hypothesis that ABC-containing cART regimens carry a greater risk of MI or major cardiovascular events relative to comparator cART.

Increased Platelet Reactivity in HIV-1–Infected Patients Receiving Abacavir-Containing Antiretroviral Therapy

Current or recent use of abacavir for treating human immunodeficiency virus type 1 (HIV-1) infection has been associated with increased rates of myocardial infarction (MI). Given the role of platelet aggregation in thrombus formation in MI and the reversible nature of the abacavir association, we hypothesized that patients treated with abacavir would have increased platelet reactivity. In a prospective study in adult HIV-infected patients, we determined associations between antiretrovirals (ARVs), and in particular the nucleoside reverse transcriptase inhibitor abacavir, and platelet reactivity by measuring time-dependent platelet aggregation in response to agonists: adenosine diphosphate (ADP), thrombin receptor-activating peptide (TRAP), collagen, and epinephrine. Of 120 subjects, 40 were ARV-naive and 80 ARV-treated, 40 of whom were receiving abacavir. No consistent differences in platelet reactivity were observed between the ARV-naive and ARV-treated groups. In contrast, within the ARV-treated group, abacavir-treated subjects had consistently higher percentages of platelet aggregation upon exposure to ADP, collagen, and epinephrine (P = .037, P = .022, and P = .032, respectively) and had platelets that were more sensitive to aggregation upon exposure to TRAP (P = .025). The consistent increases in platelet reactivity observed in response to a range of agonists provides a plausible underlying mechanism to explain the reversible increased rates of MI observed in abacavir-treated patients.

Efficacy and safety of a switch to unboosted atazanavir in combination with nucleoside analogues in HIV-1-infected patients with virological suppression under antiretroviral therapy

Limited data are available on the use of unboosted atazanavir in combination with nucleoside reverse transcriptase inhibitors (NRTIs) in treatment-experienced HIV-infected patients. We conducted a multicentre, retrospective study among patients with plasma HIV-1 RNA levels <50 copies/mL under antiretroviral therapy who switched to unboosted atazanavir + NRTIs between January 2002 and December 2008. Virological failure during follow-up was defined as a confirmed plasma HIV-1 RNA level >50 copies/mL. Baseline risk factors for virological failure were identified using Cox proportional hazards models. A total of 886 patients were analysed. At baseline, median age was 44 years, 71.5% were males and median CD4 cell count was 490 cells/mm(3). NRTIs used in combination with atazanavir were tenofovir, abacavir and emtricitabine/lamivudine in 36.9%, 44.1% and 94.4% of patients, respectively. Median follow-up was 21 months. The 3 year probability of virological failure was 20.1%. Only a history of virological failure under NRTIs [hazard ratio (HR) 1.63, P = 0.049] and under protease inhibitors (HR 2.04, P = 0.006) were significantly associated with the risk of virological failure. Among the 431 patients without a prior history of virological failure, the 3 year probability of virological failure was 11.3%, and only hepatitis C virus co-infection (HR 2.25, P = 0.026) and abacavir use (HR 0.43, P = 0.04) were associated with the risk of virological failure. Safety of the switch was satisfactory, with improvement of the lipid profile. In patients with virological suppression and no prior history of virological failure, a switch to unboosted atazanavir in combination with NRTIs is associated with a low probability of virological failure and a good safety profile.

Cardiovascular disease in HIV infection

Highly active antiretroviral therapy (HAART) use has markedly reduced AIDS-related mortality and opportunistic illness. With improved survival, cardiovascular disease (CVD) has emerged as an important noninfectious chronic comorbidity among antiretroviral (ARV)-treated HIV-infected persons. HIV infection can impact CVD and comorbidities known to increase CVD risk. Untreated HIV can cause proatherogenic elevations in serum lipids. Chronic HIV viremia results in increases in systemic inflammation, hypercoagulation, and reductions in endovascular reactivity, all of which are at least partially reversible with virally suppressive HAART. Chronic T-cell activation can also result in adverse vascular effects. Use of some ARV drugs can impact CVD risk by causing pro-atherogenic serum lipid elevations, induction of insulin resistance, increases in visceral adiposity or subcutaneous fat loss. Abacavir use may increase myocardial infarction risk by reducing vascular reactivity and/or increasing platelet activation. Traditional risk factors such as advancing age, smoking, hyperlipidemia, and hypertension remain important predictors of CVD among HAART-treated HIV-infected persons. HIV in the HAART era is a chronic manageable condition. CVD is an important cause of morbidity among HIV-infected persons. Untreated HIV can increase CVD risk in several ways and these effects are at least partially reversible with successful treatment. Use of specific ARVs can adversely impact CVD risk but the multiple long-term benefits of chronic HIV suppression and immune reconstitution achievable with potent HAART outweigh the adverse impact upon CVD risks that they may have. Standard CVD screening and risk-reducing interventions should be routinely undertaken for HIV-infected persons.

Cardiovascular risks associated with abacavir and tenofovir exposure in HIV-infected persons

Abacavir use has been associated with cardiovascular risk, but it is unknown whether this association may be partly explained by patients with kidney disease being preferentially treated with abacavir to avoid tenofovir. Our objective was to compare associations of abacavir and tenofovir with cardiovascular risks in HIV-infected veterans. Cohort study of 10 931 HIV-infected patients initiating antiretroviral therapy in the Veterans Health Administration from 1997 to 2007, using proportional hazards survival regression. Primary predictors were exposure to abacavir or tenofovir within the past 6 months, compared with no exposure to these drugs, respectively. Outcomes were time to first atherosclerotic cardiovascular event, defined as coronary, cerebrovascular, or peripheral arterial disease; and time to incident heart failure. Over 60 588 person-years of observation, there were 501 cardiovascular and 194 heart failure events. Age-standardized event rates among abacavir and tenofovir users were 12.5 versus 8.2 per 1000 person-years for cardiovascular disease, and 3.9 and 3.7 per 1000 person-years for heart failure, respectively. In multivariate-adjusted models, including time-updated measurements of kidney function, recent abacavir use was significantly associated with incident cardiovascular disease [hazard ratio 1.48, 95% confidence interval (CI) 1.08-2.04]; the association was similar but nonsignificant for heart failure (1.45, 0.85-2.47). In contrast, recent tenofovir use was significantly associated with heart failure (1.82, 1.02-3.24), but not with cardiovascular events (0.78, 0.52-1.16). Recent abacavir exposure was independently associated with increased risk for cardiovascular events. We also observed an association between recent tenofovir exposure and heart failure, which needs to be confirmed in future studies.

Abacavir Use and Risk of Acute Myocardial Infarction and Cerebrovascular Events in the Highly Active Antiretroviral Therapy Era

Some studies have suggested that exposure to antiretroviral therapy (ART) with abacavir is associated with an increased risk of acute myocardial infarction (AMI). Using the Veterans Health Administration's Clinical Case Registry we calculated the risk of AMI and cerebrovascular events (CVA) associated with the cumulative use of abacavir and other nucleoside combinations. We also evaluated the impact of pre-existing chronic kidney disease on the selection of abacavir versus tenofovir in the last recorded ART regimen, and on highly active antiretroviral therapy-associated AMI and CVA risks. A total of 19,424 human immunodeficiency virus-infected patients contributed 76,376 patient-years of follow. After adjusting for age, hypercholesterolemia, hypertension, type 2 diabetes, and smoking, the hazard ratio (HR) for each year of abacavir use was 1.18 (95% confidence interval [CI], .92-1.50; P=.191) for AMI and 1.16 (95% CI, .98-1.37; P=.096) for CVA. Abacavir use was more common among patients with prior chronic kidney disease than was tenofovir use (12.46% versus 7.15%; P=.0001), and chronic kidney disease was associated with a significantly higher risk of AMI (HR, 2.41; 95% CI, 1.73-3.36), and CVA (HR, 1.80; 95% CI, 1.44-2.24). Compared with patients who received neither tenofovir nor abacavir, patients who received tenofovir had lower risk of AMI (HR, 0.16; 95% CI, .08-.33; P=.0001) and CVA (HR, 0.22; 95% CI, .15-.32; P=.001). Use of abacavir was associated with lower risk of CVA (HR, 0.60; 95% CI, .45-.79). We observed no association between cumulative or current abacavir use and AMI or CVA. Abacavir use was more common than was tenofovir use among patients with prior chronic kidney disease, and chronic kidney disease independently predicted higher rates of AMI and CVA.

Coinfection with Human Immunodeficiency Virus and Hepatitis C Virus: Challenges and Therapeutic Advances

In the United States, approximately 30% of all human immunodeficiency virus (HIV)-positive patients are also infected with hepatitis C virus (HCV). Both viruses share similar routes of transmission. Unlike HIV or hepatitis B virus, HCV is curable if treated and the patient achieves a sustained virologic response. The impact of coinfection includes greater morbidity and mortality, with higher rates of opportunistic disease, development of cirrhosis, and death. The standard of treatment for HIV-HCV coinfection is similar to that for HCV monoinfection and consists of pegylated interferon alpha and ribavirin. As with HCV monoinfection, the best predictor of response to therapy for HIV-HCV coinfection is infection with an HCV genotype other than genotype 1 or 4. Adherence to treatment is critical for improving response to HCV therapy. However, considerable toxicities are associated with pegylated interferon alpha and ribavirin and pose particular problems in the coinfected patient. Coinfected patients are more likely to experience significant weight loss with HCV therapy. Neutropenia and anemia are both common laboratory abnormalities that necessitate dosage reductions and are concerns for development of acquired immunodeficiency syndrome-defining events. The effect of CD4(+) cell count has been evaluated both as a factor in response to HCV therapy and in stratification of risk for infection. Immunosuppression is not a contraindication to HCV therapy, although CD4(+) counts above 350 cells/mm(3) are associated with increased response rates in patients with HCV genotype 1 coinfection. Antiretroviral therapy does need to be adjusted to minimize adverse effects. Concomitant use of zidovudine is contraindicated because of its profound exacerbation of bone marrow suppression. The use of didanosine is also not indicated during HCV therapy because of the risks of hepatic decompensation. Controversy exists regarding the use of abacavir. Newer agents for HCV include the protease inhibitors telaprevir and boceprevir. Although results with the protease inhibitors are highly encouraging, their effects in coinfected patients have not been evaluated. Treatment for HCV in patients with HIV poses potential obstacles to success, but the benefits of viral eradication warrant the challenge of therapy.